Gastrointestinal motility is principally under intrinsic neural control. It has been shown that the intrinsic enteric nervous system contains the neural circuitry necessary for proper gastrointestinal motility even when extrinsic input from the central nervous system is lacking. However, malfunction or malformation of the intrinsic enteric nervous system results in a failure of proper motility. Chemical and mechanical stimuli upon the gastrointestinal mucosa alter motility patterns. Further, this chemical and mechanical stimulation can be detected as altered activity in afferent fibers within the vagus and mesenteric nerves. This would tend to indicate that there must be special receptors for these stimuli which affect the neural circuitry associated with many of the "reflexes" involved in gastrointestinal function. Since these reflexes occur in the absence of extrinsic neural input, it would follow that there must be sensory input into the intrinsic enteric nervous system which controls motility. To date there have been no studies describing the influence of mucosal sensory receptor input upon neurons within the enteric nervous system. For this reason, the present study will take segments of cat small intestine and mount them in a tissue bath where the lumen of the intestinal segments can be perfused with solutions while recordings are obtained extracellularly from neurons within the ganglia of Auerbach's plexus. The influence of intraluminal pressure and pH, changes in intraluminal osmolarity, the presence of particular foodstuffs such as carbohydrates and amino acids, and the actions of pharmacological agents upon functioning in these neurons will be investigated. It is expected that research of this type will fill a gap in our present understanding of the sensory input to the reflexes involved in the control of gastrointestinal motility.